Active participation of GPs with the performance of point-of-care tests in the clinic is accompanied by a drastic reduction of antibiotic use in RTIs, primarily in infections considered as mainly viral.

This before-after study aimed to evaluate the effect of two interventions on lowering the prescription of antibiotics in lower respiratory tract infections (LRTI) in Spain.General practitioners (GPs) registered all cases with LRTIs over 3-week periods before and after an intervention Intervention led to a reduction in the prescription of antibiotics, mainly when CRP testing was available.

Physicians with access to CRP tests significantly reduced antibiotic prescription in patients with rhinosinusitis.

Background: Rheumatoid arthritis (RA) is the most frequent autoimmune disease involving the joints. Although anti-TNF therapies have proven effective in the management of RA, approximately one third of patients do not show a significant clinical response. The objective of this study was to identify new genetic variation associated with the clinical response to anti-TNF therapy in RA. Methods: We performed a sequential multi-omic analysis integrating different sources of molecular information. First, we extracted the RNA from synovial biopsies of 11 RA patients starting anti-TNF therapy to identify gene coexpression modules (GCMs) in the RA synovium. Second, we analyzed the transcriptomic association between each GCM and the clinical response to anti-TNF therapy. The clinical response was determined at week 14 using the EULAR criteria. Third, we analyzed the association between the GCMs and anti-TNF response at the genetic level. For this objective, we used genome-wide data from a cohort of 348 anti-TNF treated patients from Spain. The GCMs that were significantly associated with the anti-TNF response were then tested for validation in an independent cohort of 2,706 anti-TNF treated patients. Finally, the functional implication of the validated GCMs was evaluated via pathway and cell type epigenetic enrichment analyses. Results: A total of 149 GCMs were identified in the RA synovium. From these, 13 GCMs were found to be significantly associated with anti-TNF response ( P < 0.05). At the genetic level, we detected two of the 13 GCMs to be significantly associated with the response to adalimumab ( P = 0.0015) and infliximab ( P = 0.021) in the Spain cohort. Using the independent cohort of RA patients, we replicated the association of the GCM associated with the response to adalimumab ( P = 0.0019). The validated module was found to be significantly enriched for genes involved in the nucleotide metabolism ( P = 2.41e-5) and epigenetic marks from immune cells, including CD4+ regulatory T cells ( P = 0.041). Conclusions: These findings show the existence of a drug-specific genetic basis for anti-TNF response, thereby supporting treatment stratification in the search for response biomarkers in RA.

intervention was beneficial for reducing the prescription of antibiotics, but was only statistically significant when the GPs were provided with RADTs.